ArticleJournal of virology2012
Attenuation of bunyamwera orthobunyavirus replication by targeted mutagenesis of genomic untranslated regions and creation of viable viruses with minimal genome segments.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 21 citations in OpenAlex.
- The La Crosse virus M segment determines virus isolate cell-to-cell spread and virulence.bioRxiv : the preprint server for biology · 2026Article
- Conserved non-coding RNA motifs influence the neuropathogenicity of Simbuviruses: Molecular dissection in the Schmallenberg virus model.PLoS pathogens · 2026Article
- Evaluation and Designing of Epitopic-Peptide Vaccine AgainstInternational journal of peptide research and therapeutics · 2022Article
- Recent Advances in Bunyavirus Reverse Genetics Research: Systems Development, Applications, and Future Perspectives.Frontiers in microbiology · 2021Review
- Mutagenic Analysis of Hazara Nairovirus Nontranslated Regions during Single- and Multistep Growth Identifies both Attenuating and Functionally Critical Sequences for Virus Replication.Journal of virology · 2020Article
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- A Review of Bunyamwera, Batai, and Ngari Viruses: UnderstudiedFrontiers in veterinary science · 2018Review
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- In memoriam--Richard M. Elliott (1954-2015).The Journal of general virology · 2015Article
- Genetic analysis of members of the species Oropouche virus and identification of a novel M segment sequence.The Journal of general virology · 2015Article
- Flexibility of bunyavirus genomes: creation of an orthobunyavirus with an ambisense S segment.Journal of virology · 2015Article
- Evolution of the Bunyamwera virus polymerase to accommodate deletions within genomic untranslated region sequences.Journal of virology · 2015Article
- Evolutionary reversion of live viral vaccines: Can genetic engineering subdue it?Virus evolution · 2015Article
- Orthobunyaviruses: recent genetic and structural insights.Nature reviews. Microbiology · 2014Review
- The consequences of reconfiguring the ambisense S genome segment of Rift Valley fever virus on viral replication in mammalian and mosquito cells and for genome packaging.PLoS pathogens · 2014Article
- Genome sequence analysis of in vitro and in vivo phenotypes of Bunyamwera and Ngari virus isolates from northern Kenya.PloS one · 2014Article
- Establishment of a reverse genetics system for Schmallenberg virus, a newly emerged orthobunyavirus in Europe.The Journal of general virology · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Bunyamwera virus (BUNV) is the prototype virus for both the genus Orthobunyavirus and the family Bunyaviridae. BUNV has a tripartite, negative-sense RNA genome. The coding region of each segment is flanked by untranslated regions (UTRs) that are partially complementary. The UTRs play an important role in the virus life cycle by promoting transcription, replication, and encapsidation of the viral genome. Using reverse genetics, we generated recombinant viruses that contained deletions within the 3' and/or 5' UTRs of the L or M segments to determine the minimal UTRs competent for virus viability. We then generated viruses carrying deleted UTRs in all three segments. These viruses were grossly attenuated in tissue culture, being significantly impaired in their ability to produce plaques in BHK cells, and had a reduced capacity to cause host cell protein shutoff. After serial passage in tissue culture, some viruses partially recovered fitness, generating higher titers and producing larger plaques. We determined the complete nucleotide sequence for each virus. The deleted UTR sequences were maintained, and no amino acid changes were observed in the nonstructural proteins (NSs and NSm), the nucleocapsid protein (N), or the Gn glycoprotein. One virus had a single amino acid substitution in Gc. Three viruses contained amino acid changes in the viral polymerase that mostly occurred in the C-terminal domain of the L protein. Although the role of this domain remains unknown, we suggest that those changes might be involved in the evolution of the polymerase to recognize the deleted UTRs more efficiently.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.